Sentence examples for oral tumors from inspiring English sources

Our results showing that EMMPRIN also regulated uPA in oral tumors and colocalized with it in the tumoral tissues where both EMMPRIN and uPA were overexpressed suggest that this pathway may play an important role in oral tumor progression.

Bannas et al. showed an incremental value of gantry tilt on the reader's sensitivity of detecting oral tumors as gantry tilt redistributed the metal artifacts to other locations outside of the slices where the tumor was [15].

We used these two primary oral tumors to study NK cell function.

Our recent findings indicated that monocytes protect oral tumors via NFκB dependent and independent pathways (manuscript submitted).

Thus, UCLA-OSCSCs, which are less differentiated oral tumors, are significantly more susceptible to NK cell mediated cytotoxicity; however, their differentiated counterparts UCLA-OSCCs are significantly more resistant.

To extend our findings to patient derived oral tumors, UCLA-OSCC and UCLA-OSCSCs were tested for their sensitivity or resistance to NK cell mediated cytotoxicity.

It appears that (1) a non-attenuated strain of HSV-1 can inhibit the growth of an aggressive malignant oral tumor, but only to a limited extent and (2) inhibition depends on the ability of the virus to replicate in the tumor.

These results also indicated that IL-6 secretion in oral tumor cells is regulated by the function of NFκB.

Thus, transduction of UCLA-OSCCs and HOK-16B cells with IκBαM or IκB S32AS36A) super-repressor constructs exhibited the same functional profiles as those seen in transfected HEp2 oral tumor cells with IκB S32AS36A) super-repressor construct [19], [20].

CAL27 and SCC4 were provided by Laboratory of Oral Tumor and Oral Biology, Shanghai Key Laboratory of Stomatology, Shanghai, China.

Our results suggest that the upregulation of uPA contributes to EMMPRIN's effect in promoting oral tumor invasion.